(DOC), corticosterone (B), and 18-hydroxydeoxycorticosterone (18-OHDOC) have a major role in regulating body electrolyte composition and blood pressure. The plasma measurement of 18-hydroxycorticosterone (18-OHB), the major penultimate precurosr of A, in addition to the earlier ones, DOC and B, is being used to further hyperplasia and hyperaldosteronism. 18-PHB levels are always high (greater than 100 ng/dl) and B and DOC elevations occur only in patients with adenoma. A decreasing plamsa potassium concentration reduces conversion of 18-OHB to A. The continued administration of ACTH in superphysiologic doses produces three patterns. DOC rises and remains elevated. B & 18-OHDOC show an initial rise followed after 24 hrs by a reduction to 28-60% of initial peak values. Both A and 18-OHB rise during first 24 hrs and then return to near control levels. ACTH impedes 11 beta and 18-hydroxylation as the mechanism for reduction of aldosterone and 11 beta and 18-hydroxylation as the mechanism for reduction of aldosterone and 11 beta and and 18 hydroxylations are likely to be the same enzyme. ACTH is likely to have inhibitory activity on aldosterone production at physiologic levels.